Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Proopiomelanocortin (POMC) is posttranslationally processed in the intermediate lobe of the pituitary to both N-terminally acetylated and nonacetylated forms of alpha MSH and beta-endorphin (beta END). N-Acetylation substantially modifies the physiological responses produced by both peptides, suggesting that the activity of the peptide acetyltransferase, which posttranslationally acetylates beta END and des-acetyl-alpha MSH, may play an important role in defining the biological activity of the secretory products of the intermediate pituitary lobe. The present results demonstrate that peptide acetyltransferase activity is induced by treating rats chronically with the dopamine receptor antagonist haloperidol. Haloperidol administration produced parallel and essentially equivalent increases in acetyltransferase activity, POMC mRNA levels, and the content and secretion of POMC-derived peptides in the neurointermediate pituitary. Time-course and dose-response studies further demonstrated that acetyltransferase activity covaried with POMC mRNA and peptide levels. Chronic treatment with the dopamine receptor agonist bromocriptine had the opposite effects; it lowered acetyltransferase activity, POMC mRNA levels, and alpha MSH and beta END immunoreactivities. Subcellular fractionation showed that acetyltransferase activity was localized in three subcellular compartments corresponding in density to secretory vesicles, rough endoplasmic reticulum and Golgi apparatus, and cytosol. Haloperidol treatment significantly increased the specific activity of the secretory vesicle-associated acetyltransferase without affecting the specific activity of the enzymes present in the endoplasmic reticulum or cytosol. Together, these data indicate that peptide acetyltransferase activity and POMC biosynthesis are coregulated.
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PMID:Coordinate regulation of peptide acetyltransferase activity and proopiomelanocortin gene expression in the intermediate lobe of the rat pituitary. 293 33

The involvement of beta-endorphin (beta-END) in the long-lasting antagonistic effect of caerulein (CLN) on amphetamine (AMP) hyperactivity in rats was investigated. Injection of beta-END antiserum into the lateral ventricle or the nucleus accumbens abolished the CLN effect, whereas the injection of normal rabbit serum had no effect on the susceptibility to AMP for about 2 weeks, as observed in intact rats. Moreover, the CLN effect was blocked by long-term dexamethasone treatment, which inhibits beta-END synthesis. These findings indicate that beta-END in the nucleus accumbens plays an important role in producing the long-lasting effect on CLN, suggesting that dopamine release induced by AMP in the nucleus accumbens is presynaptically inhibited by opiate receptors activated by beta-END.
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PMID:Further evidence for beta-endorphin involvement in the long-lasting antagonistic effect of caerulein on amphetamine hyperactivity in rats. 293 79

Intraventricularly-administered beta-endorphin (beta-END) suppresses receptive and proceptive behaviors of the ovariectomized, estrogen-progesterone-primed rat. This rat model was used in a four-way choice paradigm to investigate the behavioral specificity and motivational aspects of sexual suppression by beta-END. The experimental females showed a preference to associate with a sexually active 'stud' male over the other incentive animals as shown by significantly more approaches to and nose pokes into the stud male compartment. beta-END did not alter that choice preference. Rather, there was a decrease in overall social interaction after beta-END treatment, as shown by decreased total nose pokes. This overall decrease in social motivation, which was blocked by subcutaneous naloxone injection, was not specific to the stud male. It was not a result of akinesia, since total movement among the inner alleys was significantly higher after beta-END treatment, an effect also reversed by naloxone. These data suggest that intraventricular beta-END may act to suppress sociosexual motivation as a whole rather than sexual activity specifically.
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PMID:Effect of beta-endorphin on sociosexual proclivity in a choice paradigm. 293 66

Intraventricular (i.c.v.) administration of beta-endorphin (beta-END) has been shown to suppress lordosis behavior in ovariectomized (OVX) estrogen-progesterone (EP) primed rats, but the behavioral specificity of this effect is not known. Using OVX EP-primed rats, the present study assessed the effect of i.c.v. beta-END on proceptive behavior as well as on lordosis (receptive) behavior, and attempted to discern whether the sexual effects were secondary to generalized nonspecific behavioral effects. Doses of 0.5-4 micrograms beta-END (human) significantly suppressed lordosis behavior. Doses of 1 and 4 micrograms were used in experiments which measured proceptive behaviors (presentations and ear wiggling), and both doses abolished or nearly abolished the display of these behaviors. Administration of inactive peptide (a protein digest) had no effect on sexual behavior. Neither 1 nor 4 micrograms beta-END elicited measurable catalepsy. In a series of tests for responsiveness to general somatosensory stimuli, 1 microgram had no effect on responsiveness while 4 micrograms had minor effects, even though sexual activity was severely diminished after both doses. Blood pressure was unaltered by infusion of beta-END (1 microgram), although there was a significant reduction in heart rate. When open field behavior was tested in conjunction with sexual behavior, ambulation and rearing were significantly decreased after beta-END treatment as compared with saline treatment. However, simple linear correlation tests showed a lack of correlation between the changes in open field behavior and the changes in sexual behavior, indicating that the effects of beta-END on the two types of behavior may be unrelated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Suppression of receptive and proceptive behavior in ovariectomized, estrogen-progesterone-primed rats by intraventricular beta-endorphin: studies of behavioral specificity. 294 Apr 71

Immunoreactive beta-endorphin (ir-beta-END) concentrations were measured in the hypophysial portal plasma of the male rat under urethane anesthesia. On the basis of immunochemical studies and gel filtration chromatography it appears that ir-beta-END in rat hypophysial portal plasma is primarily beta-endorphin (beta-END) and not beta-lipotropin (beta-LPH). In addition, much of the ir-beta-END in portal plasma may be of pituitary origin since acute hypophysectomy resulted in approximately an 80% decrease in the portal plasma concentration of ir-beta-END. Nevertheless, in anesthetized animals that had been hypophysectomized acutely, portal plasma concentrations of ir-beta-END were still 5 times those in systemic plasma, indicative of hypothalamic secretion of the peptide. The administration of morphine sulfate (3 mg/kg, i.v.) resulted in a decrease of ir-beta-END concentrations from 3,157 +/- 547 pg/ml to 1,044 +/- 250 pg/ml. This effect was blocked by naltrexone (1 mg/kg, s.c.) pretreatment. Capsaicin (10 micrograms), which, when infused into the lateral cerebral ventricle of the rat, has been shown to decrease the amount of beta-END in the hypothalamus, but not elsewhere in the central nervous system, selectively decreased the concentration of ir-beta-END in portal plasma without changing systemic ir-beta-END concentrations. These studies indicate that ir-beta-END in portal plasma is probably beta-END which is derived from neurons in the hypothalamus. Moreover, it is concluded that the regulation of the release of ir-beta-END from these neurons involves opiate receptor mechanisms. The inhibitory influence of opiates on ir-beta-END secretion may be indicative of a classical feedback regulation of ir-beta-END-containing neurons.
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PMID:Morphine or capsaicin administration alters the secretion of beta-endorphin into the hypophysial portal vasculature of the rat. 294 26

Using the microdissection technique combined with the pre-embedding immunostaining method, beta-endorphin immunoreactivity (beta-END-IR) was noted within ring-shaped elements lying singly or in groups in nerve processes of the duodenal myenteric plexus of the rat. The beta-END-IR was noted as a strongly electron-dense precipitate rim on the inner surface of these elements. The membrane of the ring-shaped element as well as the beta-END precipitate rim were strikingly often unilaterally interrupted at the same site. Some of the ring-shaped beta-END-positive elements were noted within large osmiophilic bodies. The beta-END immunoreactive ring structure was 60-300 nm in diameter and possessed an empty electron-lucent space as well as a thin electron-dense membrane. The osmiophilic bodies were pleormorph, had a mean diameter of 250 nm and revealed thick electron-opaque membranes. Their inner spaces were homogenously filled with electron-dense materials. These findings might indicate that the beta-END-IR-containing ring-shaped elements represent receptosomes and that the pleomorph osmiophilic bodies are identical to lysosomes.
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PMID:beta-Endorphin is contained within presumptive receptosomes and lysosomes of the myenteric plexus of the rat. 294 63

A specific RIA for beta-endorphin (B-END) was developed to measure horse plasma levels of B-END-like material (B-END-LI) during exercises and shipping. Three exercise speeds and durations were: trot at 260-300 m/min for 10 min; slow gallop at 390-420 m/min for 5 min and fast gallop at 700-800 m/min for 2 min. Blood samples were taken from 4 horses before, immediately after, 30 and 60 min after exercise. Trotting increased plasma B-END-LI from a basal level of 109 +/- 7 pg/ml to 172 +/- 22 at the end of exercise and returned to 127 +/- 17 and 107 +/- 10 pg/ml at 30 and 60 min after exercise. Similar results were obtained in slow gallop (121 +/- 6 to 210 +/- 17 then 155 +/- 8 and 131 +/- 11 pg/ml). However, fast gallop caused the greatest increase (352%) in B-END-LI to concentrations of 544 +/- 93 pg/ml and 276 +/- 74 pg/ml at 5 and 30 min after exercise. Plasma B-END-LI returned to 199 +/- 46 pg/ml in 1 hr. Sequential exercises of trot, slow and fast gallop were conducted in 6 horses. Plasma B-END-LI were 116 +/- 19 pg/ml (pre-exercise), 198 +/- 21 (trot), 361 +/- 51 (slow gallop), 500 +/- 57 (fast gallop) and 248 +/- 29, 171 +/- 24, 143 +/- 20 and 139 +/- 21 pg/ml at 0.5, 1, 2 and 3 hr, respectively, following exercises. Transportation in horse trailer also significantly increased plasma levels of B-END-LI from a basal level of 138 +/- 12 to 196 +/- 24 pg/ml within 30 min and this levels were maintained at 45 min (177 +/- 3 pg/ml). Plasma levels of B-END-LI began to decline at 60 min of shipping. These results showed that plasma B-END-LI was increased in all speeds of exercise and by shipping and returned to pre-exercise and pre-shipping level in 30 min except fast gallop which returned to pre-exercise level in 1 hr.
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PMID:Running and shipping elevate plasma levels of beta-endorphin-like substance (B-END-LI) in thoroughbred horses. 295 72

An in vitro perifusion system was used to investigate immunoreactive beta-endorphin (beta-END-I) release from adult human hypothalami in response to dopamine (DA) and the DA receptor antagonist haloperidol (HAL). Administration of a 1 microM pulse of DA consistently elicited a mean (+/- SE) 88 +/- 9% increase (p less than 0.05, n = 5) in beta-END-I release, whereas 1 microM HAL had no effect. Administration of 1 microM DA during three perifusions in which 1 microM HAL was added to the medium failed to alter basal beta-END-I release. In contrast, DA did evoke an acute 230 +/- 31% increase (p less than 0.05) in beta-END-I release during three matching perifusions with medium containing the alpha-adrenergic antagonist phentolamine. These studies demonstrate that DA can stimulate in vitro release of beta-END-I from the adult human hypothalamus by a DA receptor mediated mechanism.
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PMID:Neurosecretion of human hypothalamic immunoreactive beta-endorphin: in vitro regulation by dopamine. 295 10

The presence of beta-endorphin-like immunoreactivity (beta-END-LI) in human gallbladder and its release were examined by means of radioimmunochemical measurements and immunohistochemical stainings. beta-END-LI was detected in the gallbladder (27.2 +/- 3.2 ng/g wet weight, mean +/- S.E.). The immunoreactivity in beta-END-LI extracted from the gallbladder was similar to that of synthetic beta-END, judging from the result of its inhibition curve parallel to that of the synthetic substance in the radioimmunoassay (RIA) system. On gel-filtration chromatography of a gallbladder extract, two components of beta-END-LI were found; one eluted on a position of beta-lipotropin (beta-LPH) and another on a position of synthetic beta-END. Specific beta-END-LI positive cells were detectable in metaplastic mucous glands. When human gallbladder mucosa was perfused with a solution of 10(-8) M or 10(-6) M cholecystokinin octapeptide (CCK-8), the release of beta-END-LI from mucosa into the perfusate increased 2-3 fold. These results indicate that beta-END-LI present in human gallbladder is released by the direct action of CCK-8 on the gallbladder mucosa and suggest that it may have a physiological or pathophysiological role.
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PMID:Beta-endorphin in the human gallbladder. 295 71

Changes in plasma concentrations of corticosterone and beta-endorphin (beta-END) were determined in male rats after treatment with the selective 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) or the non-selective 5-HT agonist 6-chloro-2-(1-piperazinyl)pyrazine (MK-212). The administration of either 8-OH-DPAT or MK-212 increased plasma concentrations of both corticosterone and beta-END in a dose-related manner. The corticosterone and beta-END responses to 8-OH-DPAT were antagonized by spiperone and (-)-pindolol, both of which have been shown to have high affinity for the 5-HT1A binding site. In contrast, antagonist which are selective for the 5-HT2 receptor or non-selective 5-HT antagonists were without effect on the hormone responses to 8-OH-DPAT. The MK-212-induced increase in plasma concentrations of corticosterone and beta-END were not affected by treatment with the 5-HT1A antagonists spiperone and (-)-pindolol. However, the corticosterone and beta-END responses to MK-212 were attenuated by the selective 5-HT2 antagonists ketanserin, ritanserin and altanserin, as well as by the non-selective 5-HT antagonist metergoline. It is concluded that stimulation of either 5-HT1A or 5-HT2 receptors results in an activation of the hypothalamic-pituitary-adrenal axis in the rat.
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PMID:Stimulation of corticosterone and beta-endorphin secretion in the rat by selective 5-HT receptor subtype activation. 295 14


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